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. Author manuscript; available in PMC: 2009 Sep 15.
Published in final edited form as: J Immunol. 2008 Sep 15;181(6):3974–3983. doi: 10.4049/jimmunol.181.6.3974

Figure 1. Rapamycin treatment delays wound closure and impairs skin γδ T cell wound healing functions.

Figure 1

Wound closure was monitored on mice administered rapamycin as compared to vehicle control (A). Rapamycin-treated mice exhibited a delay in wound closure as compared to those treated with vehicle. Data are mean ± SEM and representative of three experiments. At least six mice per condition have been examined in each experiment. (B) Representative images from wounds acquired four days post-wounding. (C) Percent of observed wounds remaining open 10 days post-wounding. Data are mean ± SD. (D) Rapamycin impairs wound closure in skin from wildtype mice to a similar degree as skin from untreated TCRδ−/− mice using a skin organ culture system. (E). Rapamycin inhibits the ability of 7–17 skin γδ T cells to restore normal wound closure to TCRδ−/− skin in organ culture. Data in skin organ cultures are mean ± SEM and representative of at least three experiments. *P < 0.05, **P < 0.005 versus vehicle control (2-tailed, unpaired Student’s t test).